Amnesia is a debilitating condition that burdens not only the affected individual but their loved ones as well. In order to develop effective treatments for amnesia, the neural mechanism underlying long term memory storage, or consolidation, needs to be understood. Several theories exist regarding memory consolidation. One such theory, called the standard consolidation theory (SCT), posits that memories are initially retained in hippocampal-cortical networks which are then gradually distributed to cortico-cortical networks as a more permanent form of storage. Behavioral lesion studies using the trace eyeblink conditioning (EBC) paradigm have provided support for SCT, showing dorsal hippocampal (HP) functioning is essential for acquisition but not retention of the paradigm, whereas medial prefrontal cortex (mPFC) functioning is critical for retention but not acquisition of the paradigm. Despite these findings that conform to SCT, electrophysiological evidence in support of SCT remains scarce. Only a handful of studies have examined dorsal HP or mPFC single neuron activity during trace EBC but none have examined activity from both of these regions simultaneously within the same subject over a time frame that examines both recently and remotely acquired trace EBC. In addition, tracing studies show no monosynaptic connections that directly link the dorsal HP to the mPFC. Thus, it remains unclear 1) whether the firing patterns of dorsal HP and mPFC neurons conform to SCT in a time-dependent manner and 2) how dorsal HP memory traces are transferred to the mPFC via consolidation as suggested by SCT. Recent anatomical tracing studies have shown that the dorsal HP may communicate with the mPFC via the anterior thalamus (AT), suggesting a dorsal hippocampal-anterior thalamic-medial prefrontal (dHP-AT-mPFC) circuit may be responsible for the consolidation of trace EBC. Our proposed research aims to first, investigate the firing characteristics of neurons within the dHP-AT-mPFC circuit and whether they support SCT (aim 1), then aims to elucidate the functional role of the AT in trace EBC (aim 2). Specifically, we will simultaneously record single neuron activity from the dorsal HP, AT, and mPFC within the same subjects as they undergo trace EBC acquisition and retention training. In accordance with SCT, we hypothesize dorsal HP and AT neurons will exhibit robust activity during acquisition, whereas mPFC neurons will exhibit greater activity during retention sessions. Preliminary results demonstrate a greater involvement of AT during acquisition of trace EBC, suggesting its role as a relay that transfers HP memory traces to the mPFC. We will further test this premise by observing the effects of temporally precise optogenetic inactivation of AT nuclei on behavioral performance during trace EBC acquisition and retention. We hypothesize that inactivation of AT will result in impaired retention of trace EBC but not acquisition by blocking the transfer of HP memory traces to the mPFC. Results may provide electrophysiological evidence in support or in opposition of SCT and further provide insight into the role of the dHP-AT-mPFC circuit in trace EBC and memory consolidation.